MULTI VALVULAR HEART DISEASE clinical presentation

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APPROACH TO THE VARIOUS MULTIVALVULAR HEART DISEASES IN CLINICAL GROUNDS

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MULTI VALVULAR HEART DISEASE clinical presentation

  1. 1. MULTI VALVULAR HEART DISEASE PROF.M.K.SUDHAKAR SRMC
  2. 2. OBJECTIVES  A CLINICAL SHORT CASE DISCUSSION  APPROACH TO THE VARIOUS MULTIVALVULAR HEART DISEASES IN CLINICAL GROUNDS.
  3. 3. CASE PRESENTATION.
  4. 4. GENERAL EXAMINATION  46 yr / male  Conscious , Oriented to time, place and person  Weight – 60 kg  Height – 162.5 cm  Arm span – 145 cm  BMI – 22.8 kg/m2
  5. 5.  Vitals  Temperature - 98.2 F  Pulse  80/min, Regular,  large volume,  Collapsing in nature(water hammer pulse)  Bis feriens in character,  Carotid thrill +.  Normal vessel wall  No radio-radial or radio-femoral delay  All peripheral pulses are well felt  No apex- pulse deficit noted.
  6. 6.  110/50 mm of Hg over right brachial artery in supine position  110/50mm of Hg over Lt. brachial artery  Systolic BP measured in lower limb is 160 mm of Hg  Hill’s sign - positive ( systolic BP difference between upper & lower limbs is 50 ) Blood Pressure
  7. 7.  JVP – elevated 5 cms above the sternal angle, but the waveforms masked by carotid pulsations in neck.  Respiration - Rate- 17/min, Regular, Abdomino-thoracic type  No other peripheral signs of AR.  No P I C C L E.  No external markers of Rheumatic fever / Infective Endocarditis  Fundus Examination – Normal
  8. 8. CARDIOVASCULAR SYSTEM
  9. 9. INSPECTION  Chest symmetrical, no spinal or chest deformity noted  Trachea appears to be in midline  Carotid pulsations are visible in the neck.  Apical impulse is visible in left 5th intercostal space in Midclavicular line confined to single intercostal space.  Visible pulsations noted in left parasternal area.  Parasternal heave is visible.  No sinus , dilated veins over chest wall.  A healed surgical scar of 15 cms in the left thoracic wall extending from mid clavicular line(6 ICS) to the post axillary line.
  10. 10. PALPATION  Trachea centrally placed.  Apex beat localized in the Left 5th Intercostal space Midclavicular line confined to single Intercostal space, tapping in nature, systolic thrill palpable.  Parasternal heave felt and not obliterable (grade 3)  Systolic thrill noted in aortic area and all over precordium.  Palpable P2 noted in pulmonary area.  Supra sternal and epigastric pulsations are felt.
  11. 11. Aortic Area  S1 heard  A2 soft.  A harsh ejection systolic murmur occupying almost of entire systole ; crescendo-decrescendo in nature with delayed peaking, of grade 4 intensity conducted to both carotids which is best audible with diaphragm of stethoscope in sitting and leaning forward position with breath held in expiration  No ejection click noted.  Dynamic auscultation:  murmur is augmented on squatting  Reduces on standing and isometric hand grip.
  12. 12.  Pulmonary Area:  S1heard  P2 loud and s2 single.  Systolic Crescendo decrescendo murmur same as heard in aortic area best heard in expiration with pt leaning forward.  No ejection click noted.  Dynamic auscultation:  murmur is augmented on expiration; squatting and reduced on isometric hand grip.
  13. 13. 2nd Aortic Area ( Erb’s Area )  S1 heard  A2 soft  A harsh ejection systolic murmur occupying almost of entire systole ; crescendo-decrescendo in nature with delayed peaking, of grade 4 intensity conducted to both carotids which is best audible with diaphragm of stethoscope in sitting and leaning forward position with breath held in expiration
  14. 14.  A grade 3 high pitched , blowing , early diastolic decrescendo murmur which is best audible with diaphragm of stethoscope in sitting and leaning forward position with breath held in expiration .  No ejection click noted.  Dynamic auscultation:  The early diastolic murmur is augmented on isometric hand grip and expiration.
  15. 15.  Tricuspid Area:  S1 , S2 heard  A High pitched Pan systolic murmur grade 4 intensity ;best heard with the diaphragm which increases on inspiration is heard.  No s3,s4 heard.
  16. 16. Mitral Area:  S1 S2 heard.  S1 loud.  Low pitched rough rumbling mid diastolic murmur of grade 3 intensity noted at the apex with the bell of the stethoscope with best heard in left lateral position and pt in expiration.  A high pitched holo systolic murmur is noted of grade 4 intensity radiating from the tricuspid area confirmed by inch auscultation. Which increases on inspiration.  No opening snap heard.  No s3 ,s4 heard.
  17. 17. OTHER SYSTEMS  Respiratory System:  Bilateral normal vesicular breath sounds heard  No added sounds  Abdominal System:  Soft , Non tender , No organomegaly  No ascites  Nervous System:  No focal neurological deficit
  18. 18. CLINICAL DIAGNOSIS  Anatomical: Mitral and Aortic valves with tricuspid valve.  Etiology :Acquired Rheumatic Valvular Heart Disease  Pathological:  Severe mitral re stenosis  Severe aortic stenosis  Moderate aortic regurgitation  Functional tricuspid regurgitation.  Complication : Pulmonary hypertension  Patient is in sinus rhythm  No evidence of Cardiac failure  No evidence of Infective endocarditis  No evidence of Thromboembolic event
  19. 19. 1.What are the common causes of Multivalvular heart diseases ?
  20. 20.  Multivalvular lesions are almost always due to Rheumatic fever  Collagen vascular diseases or myxomatous degeneration are rare causes
  21. 21.  Significant stenosis at multiple valves are usually Rheumatic  Significant regurgitation at multiple valves are usually Non Rheumatic  Significant stenosis and regurgitation together are usually rheumatic.
  22. 22. MVD  Quadrivalvular disease is most likely due to combination of causes – congenital , rheumatic, infective, degenerative disease  A unitary cause for quadrivalvular disease is either rheumatic or myxomatous degeneration
  23. 23. 2.What are the factors which modify the clinical presentation of MVD ?
  24. 24.  The natural history and clinical presentation of combined lesions is determined by the relative severity of each individual lesion and by chronology and chronicity of development  Proximal lesions mask the features of distal lesions
  25. 25. Non valvular Factors  Myocarditis  Volume overload states  Pressure overload states  CAD  Infective endocarditis  Arrhythmias
  26. 26.  WHEN DO U SUSPECT A MVD ?
  27. 27. MVD  Atrial fibrillation  Pulmonic hypertension  Pulmonic congestion  Systemic emboilsm
  28. 28. What is graham steel murmur?  What are the recent views on it?
  29. 29. Features of Combined AS/AR:
  30. 30. AS + AR  Apico carotid delay  S2 paradoxical split  A2 – soft or absent  S3  S4
  31. 31.  Prolonged Aortic ESM  Prolonged Aortic EDM  Austin Flint Murmur
  32. 32. Dominant AS vs Dominant AR
  33. 33. DOMINANT AS Anacrotic pulse Apex heave Systolic decapitation Systolic Ejection Click
  34. 34.  S2 reverse split  S3 – later  S4  Systolic murmur – late, loud, longer
  35. 35. DOMINANT AR  Wide pulse pressure  Pulsus bisferiens  Diffuse apical impulse  Early diastolic murmur  S3 – earlier
  36. 36. What is silent AS, severe AS?
  37. 37. SILENT AS Old age – non fused, calcified cusps Cardiac failure Severe AS AS + MS
  38. 38. SEVERE AS JVP a wave (Bernheim effect) Apico carotid delay S2 single or paradoxical split AEC absent S4 Systolic murmur - late, loud, longer Mitral pansystolic functional murmur
  39. 39. What is silent AR, severe AR?
  40. 40. SEVERE AR  Hills sign > 60 mm hg  S2 soft  S3  EDM – louder & longer  Cole Cecil murmur  Austin Flint murmur
  41. 41.  Cole Cecil murmur – AR EDM heard in the apex or axilla  Austin Flint murmur – MDM heard in severe and acute AR
  42. 42. SILENT AR  Acute AR  CCF  AR + AS  AR + MS
  43. 43. COMBINED MITRAL LESION:
  44. 44. MS + MR  Mitral valve orifice < 1.5 sq.cm MS is predominant  Mitral valve orifice > 1.5 sq.cm MR is predominant
  45. 45. MS + MR  Parasternal heave - prominence  Apical impulse - prominence  Apical MDM  Apical PSM
  46. 46. DOMINANT MS ?
  47. 47. DOMINANT MS  Parasternal lift – early systolic & brisker  Tapping apical impulse  S1 - loud  OS  MDM/LDM
  48. 48. DOMINANT MR?
  49. 49. DOMINANT MR  Parasternal impulse – slower & late systolic  Hyperdynamic apical impulse  Pansystolic murmur  S1 - soft  S3
  50. 50. WHAT IS…..  SILENT MS?  SEVERE MS?
  51. 51. SILENT MS  Severe MS with pulmonary hypertension RV enlarges and LV rotates clockwise - tight or silent MS  TS + MS  AS + MS
  52. 52. SEVERE MS  A2 OS interval - closer  MDM – longer  Severe PHT
  53. 53. What is  Silent MR?  Severe MR?
  54. 54. SILENT MR  Obesity  Emphysema  Chest wall deformity  LV infarction / dilatation  Para prosthetic leakage
  55. 55. SEVERE MR  S1 – soft  S2 – wide and variable  S3  PSM – intensity  MDM – short low pitch flow murmur.
  56. 56. MS + AS  The combination of Mitral stenosis and Aortic stenosis is almost always due to rheumatic  The combinations is usually associated with significant regurgitation at either valve  Mitral stenosis masks Aortic stenosis
  57. 57. MS + AS  Carotid pulse & Apex prominent  Parasternal heave  Loud S1  OS  Ejection systolic murmur Grade < 3/6  Mid diastolic murmur
  58. 58. MS < AS  Angina  Syncope  Carotid thrill  Apical impulse heave  Ejection systolic murmur
  59. 59. MS > AS  Dyspnea  Pulmonic hypertension  Atrial fibrillation  Systemic thromboembolism  MDM
  60. 60. MS + AR  Wide pulse pressure  Apical prominence  Parasternal impulse  Loud S1  OS  S3 S4
  61. 61.  Early diastolic murmur  Mid diastolic murmur
  62. 62. MR + AS  Geriatric – calcific  Rheumatic
  63. 63. MR + AS  AS augments the severity of MR  Systemic hypotension  Pulmonic hypertension
  64. 64. MR + AS  Hyperdynamic AI  S3 / S4  Mitral – PSM  Aortic – ESM
  65. 65. MR < AS  Angina  Syncope  Fatigue
  66. 66.  Carotid thrill  S4  Systolic murmur decreased on squatting or hand gripping
  67. 67. MR = AS  Angina  Dyspnea  Syncope  Fatigue  Pulmonic congestion  Systemic embolism
  68. 68.  Atrial fibrillation  Carotid thrill  Diffuse & sustained apical impulse  S2 soft  S3  S4
  69. 69. WHAT IS GALLIVARDIAN PHENOMENON?
  70. 70. GALLIVARDIAN PHENOMENON  An acoustic phenomenon whereby the aortic ejection systolic murmur radiates to the mitral area with reduced intensity but prolonged duration so as to be heard as a pansystolic murmur  AS often confused with MR
  71. 71.  Inch auscultation along the sash line appreciates the transformation  Sash line is an imaginary line through right carotid, aortic area, second aortic area ,mitral area
  72. 72. MR + AR  Most common cause is rheumatic with or without AS / MS  Pure MR and AR is due to connective tissue disorders with myxomatous degeneration of valve tissue when TR coexists  Infective endocarditis or chordal rupture produce regurgiation in congenital or rheumatic valve diseases
  73. 73.  When MR > AR , it attenuates AR  When AR > MR , it worsens MR  Pulmonary symptoms are earlier and severe with MR + AR combination than in isolation
  74. 74. MR + AR  MR is worsened by AR  Wide pulse pressure  Peripheral signs  Diffuse apical impulse
  75. 75.  P2  S3  S4  Mitral PSM  Aortic EDM
  76. 76. MR < AR  Wide pulse pressure  Longer EDM  Longer PSM  S4
  77. 77. MR = AR  Wide pulse pressure  Parasternal heave  Longer EDM  Longer PSM
  78. 78. MR > AR  Atrial fibrillation  Parasternal heave  Longer PSM
  79. 79. AS / AR / MS /MR  Rheumatic  Murmurs of all four hemodynamic lesions  Pulmonary congestion
  80. 80. TVD
  81. 81. TS  TS is very unusual as an isolated lesion  TS is almost always due to rheumatic valvulitis and is associated with coexisting disease of mitral and aortic valves  TS almost always coexists with MS and only rarely with predominant MR
  82. 82.  MS precedes TS  TS masks MS  TS is to be suspected when RHF persists after adequate mitral valvotomy
  83. 83. TR  Functional TR is more frequent than organic TR and is due to severe Pulmonary hypertension  Severe organic TR is almost always due to rheumatic origin and accompanies TS  Severe organic TR coexists with Mitral or Aortic valve disease
  84. 84. TS > TR  Tricuspid OS  The Tricuspid diastolic murmur increases and whereas Tricuspid systolic murmur decreases with inspiration
  85. 85. TR > TS  Tricuspid S3  The Tricuspid diastolic murmur decreases and whereas Tricuspid systolic murmur increases with inspiration
  86. 86. PVD  Pulmonic valve disease is unusual in rheumatic heart disease , when it occurs it is usually in quadrivalvular disease  Carcinoid tumor should be suspected when pulmonary and tricuspid valve lesions coexist
  87. 87. How will you investigate MVD ? History or Physical examination provides insignificant clues to recognize pulmonary valve disease in multivalvular disease
  88. 88. INVESTIGATIONS:  ECG  CXR  2D ECHO  Cardiac catheterization
  89. 89. How do you manage multivalvular diseases ?
  90. 90.  In Ideal conditions all lesions should be corrected simultaneously  In practice distal lesions are corrected first followed by proximal lesions.
  91. 91. PROCEDURES.  Valvotomy  Valvuloplasty  Valve replacement
  92. 92. THANK YOU……

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